Background The zotarolimus-eluting stent has shown larger in-stent late lumen loss compared to sirolimus-eluting stents in previous studies. However, this has not been thoroughly evaluated in ST elevation myocardial i...Background The zotarolimus-eluting stent has shown larger in-stent late lumen loss compared to sirolimus-eluting stents in previous studies. However, this has not been thoroughly evaluated in ST elevation myocardial infarction. Methods This was a prospective, randomized, controlled trial evaluating angiographic outcomes in patients presenting with ST elevation myocardial infarction, treated with zotarolimus-eluting stents or sirolimus-eluting stents. From March 2007 to February 2009, 122 patients were randomized to zotarolimus-eluting stents or sirolimus-eluting stents in a 1：1 fashion. The primary endpoint was 9-month in-stent late lumen loss confirmed by coronary angiography, and secondary endpoints were percent diameter stenosis, binary restenosis rate, major adverse cardiac events （a composite of cardiac death, non-fatal myocardial infarction, and target vessel revascularization）, and late-acquired incomplete stent apposition. Results Angiographic in-stent late lumen loss was significantly higher in the zotarolimus-eluting stent group compared to the sirolimus-eluting stent group （（0.49±0.65） mm vs. （0.10±0.46） mm, P=0.001）. Percent diameter stenosis at 9-month follow-up was also larger in the zotarolimus-eluting stent group （（30.0±17.9）% vs. （17.6±14.0）%, P 〈0.001）. In-segment analysis showed similar findings. There were no significant differences in binary restenosis rate, major adverse cardiac events, and late-acquired incomplete stent apposition. Conclusions Compared to sirolimus-eluting stents, the zotarolimus-eluting stent is associated with significantly higher in-stent late lumen loss at 9-month angiographic follow-up in the treatment of ST elevation myocardial infarction. Although there was no significant difference in 1-year clinical outcomes, the clinical implication of increased late lumen loss should be further studied.展开更多
Resistin plays an important role in the pathophysiology of obesity-mediated insulin resistance in mice.However,the biology of resistin in humans is quite different from that in rodents.Therefore,the association betwee...Resistin plays an important role in the pathophysiology of obesity-mediated insulin resistance in mice.However,the biology of resistin in humans is quite different from that in rodents.Therefore,the association between resistin and insulin resistance remains unclear in humans.Here,we tested whether and how the endocannabinoid system(ECS)control circulating peripheral blood mononuclear cells(PBMCs)that produce resistin and infiltrate into the adipose tissue,heart,skeletal muscle,and liver,resulting in inflammation and insulin resistance.Using human PBMCs,we investigate whether the ECS is connected to human resistin.To test whether the ECS regulates inflammation and insulin resistance in vivo,we used 2 animal models such as“humanized”nonobese diabetic/Shi-severe combined immunodeficient interleukin-2Rγ(null)(NOG)mice and“humanized”resistin mouse models,which mimic human body.In human atheromatous plaques,cannabinoid 1 receptor(CB1R)-positive macrophage was colocalized with the resistin expression.In addition,resistin was exclusively expressed in the sorted CB1R-positive cells from human PBMCs.In CB1R-positive cells,endocannabinoid ligands induced resistin expression via the p38–Sp1 pathway.In both mouse models,a high-fat diet increased the accumulation of endocannabinoid ligands in adipose tissue,which recruited the CB1R-positive cells that secrete resistin,leading to adipose tissue inflammation and insulin resistance.This phenomenon was suppressed by CB1R blockade or in resistin knockout mice.Interestingly,this process was accompanied by mitochondrial change that was induced by resistin treatment.These results provide important insights into the ECS–resistin axis,leading to the development of metabolic diseases.Therefore,the regulation of resistin via the CB1R could be a potential therapeutic strategy for cardiometabolic diseases.展开更多
文摘Background The zotarolimus-eluting stent has shown larger in-stent late lumen loss compared to sirolimus-eluting stents in previous studies. However, this has not been thoroughly evaluated in ST elevation myocardial infarction. Methods This was a prospective, randomized, controlled trial evaluating angiographic outcomes in patients presenting with ST elevation myocardial infarction, treated with zotarolimus-eluting stents or sirolimus-eluting stents. From March 2007 to February 2009, 122 patients were randomized to zotarolimus-eluting stents or sirolimus-eluting stents in a 1：1 fashion. The primary endpoint was 9-month in-stent late lumen loss confirmed by coronary angiography, and secondary endpoints were percent diameter stenosis, binary restenosis rate, major adverse cardiac events （a composite of cardiac death, non-fatal myocardial infarction, and target vessel revascularization）, and late-acquired incomplete stent apposition. Results Angiographic in-stent late lumen loss was significantly higher in the zotarolimus-eluting stent group compared to the sirolimus-eluting stent group （（0.49±0.65） mm vs. （0.10±0.46） mm, P=0.001）. Percent diameter stenosis at 9-month follow-up was also larger in the zotarolimus-eluting stent group （（30.0±17.9）% vs. （17.6±14.0）%, P 〈0.001）. In-segment analysis showed similar findings. There were no significant differences in binary restenosis rate, major adverse cardiac events, and late-acquired incomplete stent apposition. Conclusions Compared to sirolimus-eluting stents, the zotarolimus-eluting stent is associated with significantly higher in-stent late lumen loss at 9-month angiographic follow-up in the treatment of ST elevation myocardial infarction. Although there was no significant difference in 1-year clinical outcomes, the clinical implication of increased late lumen loss should be further studied.
基金supported by grants of the Korea Health Technology R&D Project“Korea Research-Driven Hospital(HI14C1277)”through the KHIDIfunded by the Korea Government(MHW)and by Korea Drug Development Fund funded by Ministry of Science and ICT,Ministry of Trade,Industry,and Energy,and Ministry of Health and Welfare(HN21C0524)National Research Foundation of Korea(NRF)grant funded by the Korea government(MSIT)(no.RS-2023-00228390).
文摘Resistin plays an important role in the pathophysiology of obesity-mediated insulin resistance in mice.However,the biology of resistin in humans is quite different from that in rodents.Therefore,the association between resistin and insulin resistance remains unclear in humans.Here,we tested whether and how the endocannabinoid system(ECS)control circulating peripheral blood mononuclear cells(PBMCs)that produce resistin and infiltrate into the adipose tissue,heart,skeletal muscle,and liver,resulting in inflammation and insulin resistance.Using human PBMCs,we investigate whether the ECS is connected to human resistin.To test whether the ECS regulates inflammation and insulin resistance in vivo,we used 2 animal models such as“humanized”nonobese diabetic/Shi-severe combined immunodeficient interleukin-2Rγ(null)(NOG)mice and“humanized”resistin mouse models,which mimic human body.In human atheromatous plaques,cannabinoid 1 receptor(CB1R)-positive macrophage was colocalized with the resistin expression.In addition,resistin was exclusively expressed in the sorted CB1R-positive cells from human PBMCs.In CB1R-positive cells,endocannabinoid ligands induced resistin expression via the p38–Sp1 pathway.In both mouse models,a high-fat diet increased the accumulation of endocannabinoid ligands in adipose tissue,which recruited the CB1R-positive cells that secrete resistin,leading to adipose tissue inflammation and insulin resistance.This phenomenon was suppressed by CB1R blockade or in resistin knockout mice.Interestingly,this process was accompanied by mitochondrial change that was induced by resistin treatment.These results provide important insights into the ECS–resistin axis,leading to the development of metabolic diseases.Therefore,the regulation of resistin via the CB1R could be a potential therapeutic strategy for cardiometabolic diseases.
